Exam 1; Cell Injury, Cell Death, and Cell Adaptations Flashcards

1
Q

This describes the origin of disease, including underlying cause and modifiers; WHY a disease occurs

A

etiology

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2
Q

This describes the development of disease, from molecular/cellular changes to functional and structural abnormalities; HOW a disease occurs

A

pathogenesis

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3
Q

True or False
Clinical signs and symptoms of disease are usually simultaneously associated with the biochemical changes associated with cell injury

A

False; the clinical signs and symptoms are usually several steps removed

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4
Q

What four things can cause decreased O2 (hypoxia) or no O2 (anoxia)

A

impaired absorption of oxygen
decreased blood flow (ischemia)
disease of blood or blood vessels
inadequate oxygenation of the blood

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5
Q

Decreased oxygen impairs this in the mitochondria

A

oxidative phosphorylation; which reduces the amount of ATP which reduces the ability of the plasma membrane to maintain homeostasis

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6
Q

Decrease oxygen causes a net gain of what in the mitochondria

A

a net gain of solute and an isosmotic gain in cytoplasmic water; affects of the ion pumps

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7
Q

When the mitochondria have an isosmotic gain in cytoplasmic water, what three things occur

A
  1. cell swelling with the formation of cell surface blebs
  2. swelling of mitochondria
  3. dilation of the endoplasmic reticulum that leads to detachment of ribosomes from the RER and dissociation of polysomes and decrease in protein synthesis; increasing lipid deposition
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8
Q

Reduced oxidative phosphorylation in the mito leads to an increase in what

A

glycolysis

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9
Q

What happens to the mito where there is an increase in glycolysis

A

increased production of lactic acid and inorganic phosphates which decreases pH and leads to chromatin clumping

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10
Q

This describes a reduced substrate for ATP production which can result in the same patterns as hypoxia/anoxia

A

hypoglycemia

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11
Q

The generation of ROS can be associated with what 5 different processes

A
inflammation
oxygen toxicity
chemicals
irradiation
aging
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12
Q

This type of ROS is inactivated spontaneously or by superoxide disputes (SOD) to form H2O2

A

superoxide

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13
Q

This type of ROS is detoxified by glutathione peroxidase and catalase

A

hydrogen peroxide

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14
Q

This type of ROS are generated by hydrolysis of water by ionizing radiation or by transitional metals such as Fe++ or Cu++

A

hydroxyl radicals

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15
Q

In which three ways do ROS damage cells

A

lipid peroxidation
protein cross-linking
reacts with thymidine and guanine to induce single strand DNA breaks

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16
Q

These systems in the body act to reduce the effects of ROS by blocking their initiation or by inactivating them

A

intracellular and extracellular antioxidant systems

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17
Q

What are some examples of the intracellular antioxidant system

A

SOD
catalase
glutathione peroxidase

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18
Q

What are some examples of the extracellular antioxidant system

A

vitamins E, A, C

serum proteins that bind free iron and copper

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19
Q

ROS cause what type of damage to DNA

A

single stranded breaks

typically seen in thymidine and guanine

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20
Q

How is the proper level of cytoplasmic Ca maintained

A

by protein sequestration in the cytoplasm, mito, and ER

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21
Q

High levels of Ca will activate which four degradative enzymes

A

ATPase
phospholipases
endonucleases
proteases

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22
Q

What are some additional ways a cell membrane can be injured

A
complement
cytotoxic T cells
virus
bacterial endotoxins and exotoxins
drugs
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23
Q

True or False

biochemical alterations occur prior to morphologic changes

A

True

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24
Q

The degree of cell injury is determined by what

A

physiologic state of the cell
cell type
intensity, duration and/or number of exposures to the etiological agent

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25
Cell injury may result in what four things
reversible cell injury cellular adaptations associated with changes in cell number, size, or differentiation cellular adaptations associated with abnormal accumulations cell death - necrosis or apoptosis
26
This is acute in nature and occurs when the cell cannot maintain normal homeostasis due to cell injury of short duration and minimal intensity
reversible cell injury
27
What are four common etiologies of a reversible cell injury
toxins infectious agents hypoxia thermal injury
28
What are the two morphologic changes of a cell during reversible cell injury
plasma membrane injury leads to an increased intracellular Na that leads to an isosmotic gain in water - edema organelles and cells swill, and the organ may appear pale and swollen
29
True or False | There is no signature biochemical event that equates with cell death
True
30
What five morphologic changes take place during necrosis
cell swelling protein denaturation yielding a glassy homogeneous cytoplasm organelle breakdown may result in vacuolated cytoplasm nuclei changes inflammation
31
The type of necrosis is dependent upon what
patterns of enzymatic degradation and by bacterial products when present
32
This is the most common form of necrosis
coagulative; cytoplasmic proteins are coagulated
33
What are the characteristics of coagulative necrosis
the nucleus is lost, but the eosinophilic outline of the cell is retained for a short time prior to being removed by the inflammatory response - cell outline, pink cytoplasm, anucleated cells
34
This type of necrosis is when the tissue is totally digested by the release of lysosomal enzymes during the acute inflammatory response; often associated with focal bacterial or fungal infections, also seen in the CNS
liquefactive necrosis (pus)
35
This type of necrosis is associated with M. tuberculosis infection; the tissue has a white and "cheesy" appearance on gross examination
caseous necrosis
36
This type of necrosis is common in trauma to the breast or in cases of pancreatitis; adipose tissue has a chalky white-yellow appearance. "soap bubble" histologic appearance
fat necrosis
37
What are the morphologic features of apoptosis
cell shrinkage chromatin condensation followed by fragmentation apoptotic bodies formation phagocytosis of the apoptotic bodies without a significant inflammatory response
38
What types of disorders can be caused by excess apoptosis
``` AIDS ischemia neurodegenerative diseases myelodysplasia toxin induced liver injury ```
39
What types of disorders can be caused by inhibition of apoptosis
cancer autoimmune diseases viral diseases
40
What is the mechanism of action of apoptosis
signaling control and integration execution removal of dead cells
41
What are the signaling methods involving apoptosis
direct signaling | regulation of mitrochondrial permeability
42
These genes serve as an on/off switch that regulates the permeability of the mito during apoptosis
Bcl-2 gene family
43
These Bcl genes inhibit apoptosis
Bcl-2 | Bcl-x
44
These Bcl genes stimulate apoptosis
Bax | bak
45
This is released from the outer mitochondria membrane and serves to disrupt the inhibitory function of Bcl-2 therefore FAVORING apoptosis
cytochorome c
46
Apoptosis signaling pathways converge on an autocatalytic proteolytic cascade of what, which can "execute" the cell
caspases
47
The mitochondria release this, that activated various enzymes like transglutaminases and endonucleases
Ca
48
In which ways are the dead cells removed
phagocytosis of deal cells and macrophages | there is little/no inflammation
49
How do apoptosis and necrosis differ in regards to stimuli
apoptosis - physiologic and pathologic | necrosis - hypoxia and toxins
50
How do apoptosis and necrosis differ in regards to morphology
Apoptosis - single cell, shrinkage, condensed chromatic, intact plasma membrane, apoptotic bodies necrosis - multiple cells, swelling, lysed plasma membrane, organelle disruption
51
How do apoptosis and necrosis differ in regards to the mechanism of DNA destruction
apoptosos - ATP dependent process, gene activation and endonuclease mediated DNA fragmentation necrosis - ATP independent process, random, diffuse, ROS, membrane injury
52
How do apoptosis and necrosis differ in regards to tissue reaction
apoptosis - minimal inflammation, phagocytosis of apoptotic bodies necrosis - inflammation
53
cells undergo this type of change due to persistent (chronic) stresses
adaptative changes
54
True or False | morphologic changes seldom specific to the type of persistent stress
True
55
This is a decrease in cell size and function with concurrent decrease in organ size and/or function
atrophy
56
What are some etiologies of atrophy
``` decreased workload loss of innervation decreased blood supply inadequate nutrition decreased hormonal stimulation aging local pressure ```
57
This is an increase in cell size and function with concurrent increase in organ size and/or function
hypertrophy
58
What are the etiologies of hypertrophy
increased functional demand increased or imbalanced nutrition increased hormonal stimulation
59
This is an increase in cell number with concurrent increase in organ size and/or function
hyperplasia
60
What are the etiologies of hyperplasia
hormones and growth factors | wound healing
61
This is the alteration in cell differentiation with concurrent alteration of tissue/organ function one adult cell type is replaced by another adult cell type in response to chronic stress
metaplasia
62
What are the etiologies of metaplasia
intestional; replacement of normal epithelium to intentional mucus-type cells squamous; normal columnar epithelium to stratified squamous (smokers)
63
What are the categories of cell accumulations
excess of normal cellular constituent such as H20, lipids, proteins, and carbohydrates, and pigments that may be endogenous or exogenous
64
What are the four mechanisms of intracellular accumulations
abnormal metabolism lack of an enzyme abnormal protein folding or transport ingestion of indigestible material
65
What can occur with lipid accumulation
steatosis (fatty liver); abnormal accumulation of triglycerides within the parenchymal cells of the liver, heart, kidney, and muscles
66
What can be the etiology of steatosis
``` obesity diabetes EtOH anorexia toxins protein malnutrition ```
67
What is the gross appearance of steatosis
enlarged yellow (liver)
68
What is the microscopic appearance of steatosis
hepatocytes contain clear cytoplasmic vacuoles that displace the nucleus
69
This accumulates primarily in macrophages; in the sub epithelial macrophages forming xanthoma and in the vessels forming atheromas
cholesterol
70
What is the histology of protein accumulation
eosinophilic cytoplasmic droplets, vacuoles, or aggregates
71
What are some examples of disorders of protein accumulation
``` ɑ-1-anti-trypsin deficiency mallory bodies (improper folding) neurofibrillary tangles in Alzheimers ```
72
What is the morphology of excess glycogen/glucose
clear, cytoplasmic/nuclear vacuoles
73
What are some examples of exogenous pigmentation
carbon accumulated in macrophages, anthracosis vs. pneumoconiosis tattoos
74
What are some examples of endogenous pigmentation
lipofuscin melanin hemosiderin bilirudin
75
This is an endogenous pigment that is "wear and tear" "brown-yellow granular pigment a lipoprotein complex due to ROS preoxidation of membranes
lipofuscin
76
This is an endogenous pigment that is black-brown, produced by melanocytes but accumulated in adjacent epidermal cells and in macrophages
melanin
77
This is an endogenous pigment that is yellow-brown representing aggregates of ferritin micelles; accumulation from excess iron locally due to hemorrhage.
hemosiderin
78
This is a genetic disease associated with cell death due to uncompensated hemosiderin accumulation
hemochromatosis
79
This is an endogenous pigment that is yellow-brown and is the end product of heme metabolism; it accumulates in hepatocytes and bile ducts due to hemolysis, obstructed bile flow, and/or hepatocellular disease
bilirudin